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Clinical 3 > Diabetes complications > Flashcards

Diabetes complications Flashcards

1
Q

What are the acute and chronic complications of diabetes?

A

Acute: Hypoglycemia and Hyperglycemia

Chronic Complications:
Specific (Retinopathy, Nephropathy, Neuropathy)
and
Non-specific (Coronary artery disease, stroke, peripheral artery disease, infections & amputations)

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2
Q

What are the 2 types of chronic complications>

A

Microvascular and macrovascular

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3
Q

Name and describe microvascular complications

A

Diabetic Retinopathy: Leading cause of blindness in working- age adults
Diabetic Nephropathy: Leading cause of end- stage renal disease
Diabetic Neuropathy: Leading cause of non- traumatic lower extremity amputations

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4
Q

Name and describe macrovascular complications

A

Stroke: 2- to 4-fold increase in cardiovascular mortality and stroke
Cardiovascular Disease: 8/10 diabetic patients die from CV events

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5
Q

What is the definition of hypoglycemia

A
  1. Development of neurogenic or neuroglycopenic symptoms
  2. Low blood glucose (<4 mmol/L if on insulin or secretagogue)
  3. Response to carbohydrate load
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6
Q

Name Neurogenic (autonomic) and Neuroglycopenic symptoms of hypoglycemia

A

Neurogenic: trembling, palpitations, sweating, anxiety, hunger, nausea
Neuroglycopenic: difficulty concentrating, confusion, weakness, drowsiness, vision changes, difficulty speaking, dizziness

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7
Q

What is Neuroglycopenia

A

Neuroglycopenia is a shortage of glucose (glycopenia) in the brain, usually due to hypoglycemia.

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8
Q

How does metformin and insulin affect the risk of hypoglycemia

A

T2 have taking metformin have low risk

someone taking insulin has quite a high risk

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9
Q

Describe characteristic of mild, moderate and severe hypoglycemia

A 
Mild
– Autonomic symptoms present 
– Individual is able to self-treat
Moderate
– Autonomic and neuroglycopenic symptoms 
– Individual is able to self-treat
 Severe
– Requires the assistance of another person 
– Unconsciousness may occur
– Plasma glucose is typically<2.8mmol/L
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10
Q

What happens at each stage of BG drop from 5mmol/L to 1mmol/L

A

4.4 – 4.7 mmol/L: Decreased insulin secretion
3.6 – 3.9 mmol/L: Increased glucagon, epinephrine, cortisol and growth hormone secretion
2.8 – 3.1 mmol/L: Symptoms (*Note that some patients will have symptoms >3.1 mmol/L due to the counter hormonal release;)
< 2.8 mmol/L: Reduced cognition, aberrant behavior, seizure, potential loss of consciousness and coma**
< 1.5 mmol/L: Neuronal death†

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11
Q

which 2 diabetes meds put people at increased risk of hypoglycemia

A

people treated with sulfonylureas or insulin

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12
Q

Risk factors for severe hypoglycemia in people treated with sulfonylureas or insulin

A
  • Prior episode of severe hypoglycemia
  • Current low A1C (<6.0%)
  • Hypoglycemia unawareness e.g. pregnant or elderly don’t feel the symptoms
  • Long duration of insulin therapy
  • Autonomic neuropathy
  • Chronic kidney disease
  • Low economic status, food insecurity
  • Low health literacy
  • Preschool-age children unable to detect and/or treat mild hypoglycemia on their own
  • Adolescence
  • Pregnancy
  • Elderly
  • Cognitive impairment
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13
Q

Steps to address Hypoglycemia

A
  1. Recognize autonomic or neuroglycopenic symptoms
  2. Confirm if possible (blood glucose < 4.0 mmol/L)
  3. Treat with “fast sugar” (simple carbohydrate) (15 g) to relieve symptoms
  4. RETEST in 15 minutes to ensure the BG >4.0 mmol/L and retreat (aka repeat the steps above) if needed
  5. Eat usual snack or meal due at that time of day or a snack with 15 g carbohydrate plus protein to ensure sufficient glucose reserves until next meal
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14
Q

Examples of 15 g Simple Carbohydrate

A
  • 15 g of glucose in the form of glucose tablets (recommended option-> more rapidly absorbed)
  • 15 mL (3 teaspoons) or 3 packets of sugar dissolved in water
  • 150 mL of juice or regular soft drink
  • 6 Lifesavers (1 = 2.5 g of carbohydrate)
  • 15 mL (1 tablespoon) of honey
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15
Q

Treatment of severe hypoglycemia in a conscious person

A

20-15-15 rule

  1. Treat with 20g of oral “fast sugar” (simple carbohydrate)
  2. Retest in 15 minutes to ensure the BG > 4.0 mmol/L and retreat with a further 15 g of carbohydrate if needed
  3. Eat usual snack or meal due at that time of day or a snack with 15 g carbohydrate plus protein
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16
Q

Treatment of severe hypoglycemia in an unconscious person with no IV access

A
  1. Treat with 1mg of glucagon subcutaneously or intramuscularly** (Treatment with nasal glucagon 3 mg should also be considered.)
  2. Call 911
  3. Discuss with diabetes health- care team
  4. Once conscious, eat usual snack or meal due at that time of day or a snack with 15 g carbohydrate plus protein
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17
Q

Treatment of severe hypoglycemia in an unconscious person with IV access

A
  1. Treat with 10-25g (20-50mL of D50W) of glucose intravenously over 1-3 minutes
  2. Retest in 15minutes to ensure the BG >4.0 mmol/L and retreat with a further 15 g of carbohydrate if needed
  3. Once conscious, eat usual snack or meal due at that time of day or a snack with 15g carbohydrate plus protein
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18
Q

What is one annoying thing about injectable insulin

A

It has to be reconstituted

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19
Q

Benefits of nasal glucagon

A
  • no reconstitution required
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20
Q

Name hyperglycemic complications. Which of them are more common in T1 and T2

A 
DKA = Diabetic Ketoacidosis (more common for T1)
HHS = Hyperosmolar Hyperglycemic State (more common for T2)
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21
Q

What is diabulimia

A

also known as T1ED, is an eating disorder in which people with type 1 diabetes deliberately give themselves less insulin than they need or stop taking it altogether for the purpose of weight loss.

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22
Q

What may hyperglycemia result from?

A

result from insulin deficiency or increased insulin demand
inflammation, intoxication and meds can change insulin demand and lead to DKA and HHS
stress will cause the release of glucagon, stimulating glucose release

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23
Q

Who is at risk of DKA

A
  • Age <2 years have 3x higher risk of developing DKA compared to those greater than 2 years
  • Ethnic minorities have greater risk than non-hispanic white youth.
  • Lower socioeconomic status
  • Lack of private health insurance
  • Lower parental education
  • Lower body mass index
  • Preceding infection
  • Adolescent girls (related to body image issues)
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24
Q

DKA characteristic and treatments

A
  • Ketoacidosis (ph < 7.3 and high ketones)
  • ECFV contraction
  • Milder hyperosmolarity
  • Normal to high glucose
  • May have decreased LOC
  • Beware hypokalemia (With impaired insulin action and hyperosmolality, utilization of potassium by skeletal muscle is markedly diminished leading to intracellular potassium depletion. Also, potassium is lost via osmotic diuresis causing profound total body potassium deficiency)
  • Must use insulin!!
  • Absolute insulin deficiency + increased glucagon
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25
Q

HHS characteristic and treatments

A 
• Minimal acid-base problem (pH >7.3) 
• ECFV contraction
• Hyperosmolarity
• Marked hyperglycemia
• Marked decreased LOC
• Beware hypokalemia
• May need insulin
• Relative insulin deficiency
dehydration is the main problem-> treatment is slow rehydration
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26
Q

Clinical presentation of DKA

A

Hyperglycemia
Symptoms: polyuria, polydipsia, weakness
Signs: ECFV contraction

Acidosis
Symptoms: air hunger, nausea, vomiting and abdominal pain altered sensorium
Signs: Kussmaul respiration, acetone-odoured breath altered sensorium

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27
Q

DKA vs HHS in terms of speed of manifestation

A

DKA develops very fast

HHS is slower to develop (several days)

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28
Q

All diabetics should test for ketones during:

A
  • acute illness accompanied by elevated BG
  • stress
  • consistently elevated blood glucose levels (>14 mmol/l)
  • symptoms of ketoacidosis, such as nausea, vomiting, or abdominal pain are present
  • pregnancy
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29
Q

Are ketones in urine a good predictor of levels of ketones?

A

Ketones are normally present in urine, but usually in amounts below the limit of detectability
• False positives: several sulfhydryl drugs (e.g. captopril)
• False-negatives: test strips exposed to air for extended periods of time or highly acidic specimens, such as after large intakes of ascorbic acid.
• Urine ketone tests are not reliable for diagnosing or monitoring treatment of ketoacidosis.

30
Q

What is the preferred method of measuring ketones?

A

Blood ketone testing methods that quantify ß-OH butyrate acid are preferred over urine ketone testing for diagnosing and monitoring ketoacidosis.

31
Q

What are the possible precipitation factors for DKA?

A 
• Insulin omission – MOST COMMON CAUSE of DKA
• New diagnosis of diabetes
• Infection / Sepsis
• Myocardial infarction
- Small rise in troponin may occur without overt ischemia 
- ECG changes may reflect hyperkalemia
• Thyrotoxicosis
• Drugs
32
Q

Chronic complications: specific and non-specific

A
  • Specific: Retinopathy, Nephropathy, Neuropathy

* Non-Specific: Cardiopathy (Coronary artery disease +++), Stroke, Arteritis of the lower limbs, Amputations, Infections

33
Q

_% decrease in A1C reduces the risk of complications (T2DM)

A

1% decrease in A1C reduces the risk of complications (T2DM)

34
Q

What can help to decrease A1C by one percent

A

diet

35
Q

What are the benefits of reducing A1C

A

Decrease of:

  • Lower limb amputation or secondary arterial disease deaths
  • Vascular complications
  • Cataract extraction
  • Heart failure
  • Myocardial infarction
  • Stroke
36
Q

Chronic Complications: Vision
types of complications
specific to any diabetes type?

A

• Retinopathy
- Eventually develops to some degree in most people with Type 1 and many people with Type 2. (more common in Type 2 DM on insulin vs Type 2 DM on non-insulin antihyperglycemic agents)
• Glaucoma
• Cataracts

37
Q

What are the changes that lead to retinopathy?

A

• Loss of pericytes
- Role in vessel stability and regulate control of endothelial
proliferation and angiogenesis

• Changes in the Retinal vasculature

  • Thickening of basement membrane
  • Hyperpermeability
  • Microaneurysm formation
  • Microvascular occlusion and ultimately neovascularization
38
Q

Screening for retinopathy: guidelines

A

When to initiate screening

  • Type 1 diabetes: 5 years after diagnosis in all individuals ≥15 years
  • Type 2 diabetes: children, adolescents and adults at diagnosis

If retinopathy is not present

  • Type 1 diabetes: rescreen annually
  • Type 2 diabetes: rescreen every 1 to 2 years
  • Review glycemic, BP and lipid control, and adjust therapy to reach targets as per guidelines*
  • Screen for other diabetes complications
39
Q

Difference in impact of conventional vs intensive insulin regimen on retinopathy

A

intensive has much stronger trend in reducing Retinopathy

40
Q

Define neuropathy

A

the presence of symptoms and/or signs of peripheral nerve dysfunction in people with diabetes after the exclusion of other causes

41
Q

What can accelerate neuropathy?

A

Smoking, lack of exercise, alcohol (>4 drinks/day)

42
Q

2 main types of neruopathy

A

diffuse and focal

43
Q

diffuse neuropathy

A

• Peripheral: Legs, feet, arms, hands • Autonomic/Visceral: Heart, digestive, sexual organs, urinary tract, sweat glands

44
Q

focal neuropathy

A
  • Eyes, face, mouth, hearing, pelvis, lower back, thigh, abdomen
45
Q

is neuropathy reversible

A

• Tight Glycemic control can reverse neuropathy

46
Q

intensive vs conventional insulin treatment and neuropathy

A

intensive significantly decreases neuropathy

47
Q

why is nephropathy so problematic

A

• Affects 20-30% of diabetics
• Leading cause of renal failure in US
- the problem with declinign renal function is that once your renal function declines, your choice for diabetes medication also declines

48
Q

What can increase the risk of nephropathy

A

• DM + HTN or smoking or hyperchol. increases risk

-

49
Q

Early diagnosis of nephropathy and managemnt of nephropathy

Is it reversible?

A
  • Earliest clinical evidence is persistent microalbuminuria
  • Management: control hypertension and cholesterol, limit protein to improve GFR
  • Not reversible
50
Q

How does diabetes affect the target for vascular protetcion ? EWhy

A

with diabetes we aim for tighter blood pressure control, tight LDL and may look for extra drugs if diet and lifestyle changes are not enough
Diabetes is linked with macrovascualr complications and increased CVD risk
diabetes is related to dyslipidemia, hypertension, obesity

these factors are also related to increased CVD risk

51
Q

How are control target for vascular protection altered when someone ha san increased risk for CVD

A

if someone is at risk of CVD, a more intense approach will be taken
not only behaviour and A1C will be targeted, but also LDL

52
Q

which drugs protect the heart?

A

A – ACEi or ARB
S – Statin
A – ASA if indicated
SGLT2i / GLP-1RA with demonstrated CV benefit if type 2 DM with CVD and A1C not at target

53
Q

What is the Multifaceted Vascular Protection Strategy and what are the benefits

A 
Healthy Behaviours/weight management
Smoking Cessation
Physical Activity
BP <130/80 mmHg
A1C ≤7%
Rx: Statins, ACEi/ARB, Certain Antihyperglycemic Agents

Benefits: signifiant decrease in all cause mortality, CVD mortality, CVD events, macroalbuminuria, retinopathy

54
Q

Dyslipidemia components associated with type 2 diabetes and metabolic syndrome

A
  • Increased TG and TG-rich lipoproteins
  • Increased postprandial TG
  • Low HDL-C
  • Low apo A-I
  • Decreased small HDL, prebeta-1 HDL, alpha-3 HDL
  • Increased apo B
  • Increased LDL particle number
  • Increased small, dense LDL
  • Increased apo C-III
  • Increased non-HDL-C
  • Increased oxidized and glycated lipids

there are different types of dislpipidema associated with diabetes, thus we need to adjust treatment so it would fit specifically for our client
statins really help with displipidemia-> a lot of patients are on statins

55
Q

How are statins and diebates linked

A

Diabetes>15yrs duration and age >30yr is a reason for statin prescription regardless of baseline LDL-C
This is due to the fact that many diabetic patients experience CVD so we want to prevent the risk

56
Q

how can ldl levels be decreased

A

LDL can be decreased by:

  • diet: less saturated fats; increase fibre intake
  • wegiht: excess weight is linked to increased LDL
  • physical activity
  • statins
57
Q

How is diabetes linked to mental health

A

Mental illness increases risk of diabetes and diabetic complications (Major Depressive Disorder increases the risk of Type 2 diabetes by 60%!)

this may be due to:
• Non-adherence to medication and self-care
• Functional impairment 
• Risk of complications 
• Healthcare costs
• Risk of early mortality

Diabetes can also increase the risk of mental disorder

58
Q

A1C and brain function

A

Each 1% elevation in A1C increases the risk of mild cognitive impairment (MCI) and dementia.

59
Q

Mental disorders and metabolic conditions

A

People taking high-risk psychiatric medications need regular metabolic screening
- as they can develop metabolic conditions

60
Q

Diabetes and NAFLD

A

• A large number of patients with T2DM ( >70% ) develop NAFLD with its inflammatory complication, NASH.
• The high incidence of NASH in patients with T2DM leads to further complications, such as liver cirrhosis and hepatocellular carcinoma, which are increasingly recognized.
• Medications used in the treatment of T2DM are also effective in the therapy of NASH
- treatment for NAFL is similar to diabetes -> lifestyle changes, PA, diet
- drugs that we use for diabetes are associated with improvement of liver diseases such as NAFL

61
Q

Making the Diagnosis of Hypertension in People with Diabetes

A

BP >130/80 mm Hg

Confirmed on a second occasion in either the office, home or by appropriate ambulatory measurement.

62
Q

benefits of tight BP control in diabetes

A
  • tight BP control (which still means that BP is gonna be higher than healthy people_ reduced the risk of CV events
63
Q

weight and glycemic control

A

weight loss of 5-10% can improve glycemic control

64
Q

diabetes, obesity and weight

A
  • 80-90% of people with type2 diabetes have overweight or obesity*
  • Some antihyperglycemic therapies contribute to weight gain
  • Higher BMI increases mortality
65
Q

Treatment Strategies for Obesity

A
  • Healthy behaviour interventions: Diet, activity and psychological treatments
  • Pharmacotherapy
  • Bariatric surgery
66
Q

Medications approved for the treatment of obesity in type 2 diabetes

A
  • Gastrointestinal lipase inhibitor: has side effects, weak relative weight loss and is relatively expensive. Decreases fat absorption, may require vitamin supplementation
  • GLP-1 receptor agonist: better effect on weight loss, but is also more expensive; has side effects
67
Q

Weight Effects and Antihyperglycemic Medications

A

Some Antihyperglycemic meds lead to weight gain
Others are Weight Neutral or Decrease Weight
- has to be considered and communicated during prescription

68
Q

Gastroparesis and diabetes

A
  • Neuromuscular disorder
  • Characterized by delayed gastric emptying (++solid food) in the absence of mechanical obstruction
  • Could affect 30 to 50% of patients with diabetes
  • Mean age of onset: 34 y.o. and more prevalent in women > men (4:1)
  • Increased risk of hypoglycemia
  • Recommendations: low-fiber, small frequent meals with a greater proportion of liquid calories to meet nutrition needs.
  • High protein meals and large-particle meals delay gastric emptying and should be avoided.
69
Q

Celiac disease and DM

A
  • more frequent in T1
70
Q

Dawn Phenomenon and DM

A
  • An abnormal early morning increase in blood sugar (between 4 AM – 8 AM). More common in type I DM than type 2.
  • Fasting glucose levels rise because of an increase in hepatic glucose production, which may be secondary to the midnight surge of growth hormone
71
Q

Somogyi Phenomenon/Nocturnal Hypoglycemia

A
  • Also known as rebound hyperglycemia or post hypoglycemia hyperglycemia.
  • It is a pattern of hypoglycemia’s followed by hyperglycemia. (Counterregulatory hormones stimulate gluconeogensis)
  • When it is suspected, the patient should wake between 2 and 4 am to monitor blood glucose levels.
  • Symptoms: nightmares, sweating, difficulty waking up, morning headaches….but may be asymptomatic.

Clinical 3 (17 decks)

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